Lumbar motor neuron size and number is affected by age in male F344 rats

Jacob, Jane M.

doi:10.1016/s0047-6374(98)00117-1

Cited by 54 publications

(41 citation statements)

References 28 publications

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“…We therefore interpreted any differences in dendritic spine profiles across groups as not due to variations in neuronal sampling, but rather an effect of experimental treatments. As a note, the values for maximum cell diameter, form factor, and dendritic branch lengths were similar to measurements for ␣-motor neurons that were labeled by intramuscularly injected retrograde tracers (Bose et al 2005;Crockett et al 1987;Hashizume et al 1988;Jacob 1998).…”

Section: Contusion Sci Disrupts the Dorsal Corticospinal Tractsupporting

confidence: 78%

“…We were specifically interested in motor neuron pools that innervated muscle groups in the forelimb (i.e., extensor carpi radialis) and hindlimb (i.e., plantar muscle). To identify these ␣-motor neurons, we followed a screening workflow based on data from our previous study (Tan et al 2012a) and those previously validated in rats (Crockett et al 1987;Hashizume et al 1988;Jacob 1998). We began with a broad sample population of neurons by identifying Golgi-stained ␣-motor neurons located in the ventral spinal cord in Rexed lamina IX and with soma diameters Ͼ25 m (Hashizume et al 1988;Jacob 1998).…”

Section: Animals and Spinal Cord Injurymentioning

confidence: 99%

“…To identify these ␣-motor neurons, we followed a screening workflow based on data from our previous study (Tan et al 2012a) and those previously validated in rats (Crockett et al 1987;Hashizume et al 1988;Jacob 1998). We began with a broad sample population of neurons by identifying Golgi-stained ␣-motor neurons located in the ventral spinal cord in Rexed lamina IX and with soma diameters Ͼ25 m (Hashizume et al 1988;Jacob 1998). Above the injury site (C4 -C5), we narrowed candidate neurons for analysis by selecting neurons from motor pools located in similar dorsolateral coordinates of ␣-motor neurons shown to innervate the extensor carpi radialis muscle group (ϳ1.5-2 mm deep, 1.5-2 mm lateral from midline), as we and others have demonstrated through intramuscular retrograde tracing studies (Sunshine et al 2013;Tan et al 2012a;Tosolini et al 2013).…”

Section: Animals and Spinal Cord Injurymentioning

confidence: 99%

“…Above the injury site (C4 -C5), we narrowed candidate neurons for analysis by selecting neurons from motor pools located in similar dorsolateral coordinates of ␣-motor neurons shown to innervate the extensor carpi radialis muscle group (ϳ1.5-2 mm deep, 1.5-2 mm lateral from midline), as we and others have demonstrated through intramuscular retrograde tracing studies (Sunshine et al 2013;Tan et al 2012a;Tosolini et al 2013). Below the injury site (L4 -L5), we narrowed our sampled ␣-motor neurons to those located in ventral motor pools with similar dorsolateral coordinates of motor pools known to innervate the plantar muscle (ϳ1.5-2.5 mm deep, 1.5-2.2 mm lateral from midline) as shown by retrograde tracing (Crockett et al 1987;Jacob 1998). As a refinement step for analysis a priori, we only included ␣-motor neurons for analysis that had 1) dendrites and dendritic spines that were clearly and completely impregnated, 2) dendritic branches appearing as a continuous length for at least 350 m within the tissue slice, and 3) at least one-half of the primary dendritic branches remaining within the thickness of the tissue section such that their endings were not cut and appeared to taper into a complete ending (see representative neuron in Fig.…”

Section: Animals and Spinal Cord Injurymentioning

confidence: 99%

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Dendritic spine dysgenesis contributes to hyperreflexia after spinal cord injury

Bandaru

Liu

Waxman

et al. 2015

Journal of Neurophysiology

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Bandaru SP, Liu S, Waxman SG, Tan AM. Dendritic spine dysgenesis contributes to hyperreflexia after spinal cord injury. J Neurophysiol 113: 1598 -1615, 2015. First published December 10, 2014 doi:10.1152/jn.00566.2014.-Hyperreflexia and spasticity are chronic complications in spinal cord injury (SCI), with limited options for safe and effective treatment. A central mechanism in spasticity is hyperexcitability of the spinal stretch reflex, which presents symptomatically as a velocity-dependent increase in tonic stretch reflexes and exaggerated tendon jerks. In this study we tested the hypothesis that dendritic spine remodeling within motor reflex pathways in the spinal cord contributes to H-reflex dysfunction indicative of spasticity after contusion SCI. Six weeks after SCI in adult Sprague-Dawley rats, we observed changes in dendritic spine morphology on ␣-motor neurons below the level of injury, including increased density, altered spine shape, and redistribution along dendritic branches. These abnormal spine morphologies accompanied the loss of H-reflex ratedependent depression (RDD) and increased ratio of H-reflex to Mwave responses (H/M ratio). Above the level of injury, spine density decreased compared with below-injury spine profiles and spine distributions were similar to those for uninjured controls. As expected, there was no H-reflex hyperexcitability above the level of injury in forelimb H-reflex testing. Treatment with NSC23766, a Rac1-specific inhibitor, decreased the presence of abnormal dendritic spine profiles below the level of injury, restored RDD of the H-reflex, and decreased H/M ratios in SCI animals. These findings provide evidence for a novel mechanistic relationship between abnormal dendritic spine remodeling in the spinal cord motor system and reflex dysfunction in SCI.

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Section: Contusion Sci Disrupts the Dorsal Corticospinal Tractsupporting

confidence: 78%

Section: Animals and Spinal Cord Injurymentioning

confidence: 99%

Section: Animals and Spinal Cord Injurymentioning

confidence: 99%

Section: Animals and Spinal Cord Injurymentioning

confidence: 99%

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Dendritic spine dysgenesis contributes to hyperreflexia after spinal cord injury

Bandaru

Liu

Waxman

et al. 2015

Journal of Neurophysiology

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“…Neural alterations occur at the ventral spinal cord motor neurone, peripheral nerve and neuromuscular junction in aging mammals. Age-related changes in the neuronal soma size (Liu et al ., 1996;Kanda & Hashizume, 1998) and number (Hashizume et al ., 1988;Zhang et al ., 1996;Jacob, 1998) in the spinal cord have been reported. Age-related changes in peripheral nerve have been documented in tibialis nerves of mice aged 6 -33 months (Ceballos et al ., 1999) including accumulation of collagen in the perineurium and lipid droplets in the perineurial cells, together with an increase in the number of macrophages and mast cells.…”

Section: Effects Of Age On the Neuromuscular Junctionmentioning

confidence: 97%

Neural control of aging skeletal muscle

2003

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SummaryFunctional and structural decline in the neuromuscular system with aging has been recognized as a cause of impairment in physical performance and loss of independence in the elderly. Alterations in spinal cord motor neurones and at the neuromuscular junction have been identified as evidence of denervation in skeletal muscles from aging mammals, including humans. However, the reciprocal influences of neurones on gene expression in muscle and of muscle on age-related neurodegeneration are poorly understood, and, as a result, interventions aimed at delaying or preventing degeneration of the neural component in aging muscle have been largely unsuccessful. The present article discusses the evidence for neural influence on age-related impairments of skeletal muscle, including a role in excitation-contraction uncoupling. The role of nerves in regulating the trophic actions of insulin-like growth factor-1 (IGF-1) and other neurotrophic factors is considered as a novel influence on the effects of aging on the neuromuscular junction. A better understanding of nerve-muscle interactions will allow for more rational interventions in the aging neuromuscular system.

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Human Masseter Muscle Fibers From the Elderly Express Less Neonatal Myosin Than Those of Young Adults

Cvetko¹,

Karen²,

Janáček³

et al. 2012

The Anatomical Record

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In contrast to limb muscles where neonatal myosin (MyHC-neo) is present only shortly after birth, adult masseter muscles contain a substantial portion of MyHC-neo, which is coexpressed with mature MyHC isoforms. Changes in the numerical and area proportion of muscle fibers containing MyHC-neo in masseter muscle with aging could be expected, based on previously reported findings that (i) developmental MyHC-containing muscle fibers exhibit lower shortening velocities compared to fibers with exclusively fast MyHC isoforms and (ii) transformation toward faster phenotype occurs in elderly compared to young masseter muscle. In this study, we detected MyHC isoforms in the anterior superficial part of the human masseter muscle in a sufficiently large sample of young, middle-aged, and elderly subjects to reveal age-related changes in the coexpression of MyHC-neo with adult MyHC isoforms. MyHC isoforms were visualized with immunoperoxidase method and the results were presented by (i) the area proportion of fibers containing particular MyHC isoforms and (ii) the numerical proportion of fiber types defined by MyHC-1, -2a, -2x, and -neonatal isoform expression from a successive transverse sections. We found a lower numerical and area proportion of fibers expressing MyHC-neo as well as a lower area proportion of fibers containing MyHC-1 in elderly than in young subjects. We conclude that the diminished expression of MyHC-neo with age could point to a lower regeneration capacity of masseter muscle in the elderly. Anat Rec, 295:1364Rec, 295: -1372

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Lumbar motor neuron size and number is affected by age in male F344 rats

Cited by 54 publications

References 28 publications

Dendritic spine dysgenesis contributes to hyperreflexia after spinal cord injury

Dendritic spine dysgenesis contributes to hyperreflexia after spinal cord injury

Neural control of aging skeletal muscle

Human Masseter Muscle Fibers From the Elderly Express Less Neonatal Myosin Than Those of Young Adults

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